This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Wood smoke (WS) is regulated according to the EPA guidelines for air quality, which are based on urban particulate studies. Wood smoke particulates are not the same as urban particulates, but the specific health effects of WS are not defined. A variety of studies have found increases in acute respiratory illnesses (ARI) in children in homes where biomass burning (i.e. wood) is the method of cooking. Human observations point to strong links between smoke exposure and respiratory illness, but are lacking in the cellular and molecular events that are involved. By contrast, cigarette smoke (CS) research is extensive. Recent studies have linked CS with activation of the aryl hydrocarbon receptor (AhR) and its subsequent activation of the RelB member of the NF[unreadable]B family of transcription factors. AhR is an orphan receptor that binds with dioxin and dioxin-like compounds and can promote alterations in the immune system. Several groups have described multiple types of polyaromatic hydrocarbons (PAH) in WS that are the same or similar to those found in CS. We propose to assess the effects of WS components on macrophage function using a murine pulmonary model. Wood smoke-derived alterations in macrophage function will be defined by flow cytometry, molecular biology, transgenic and null mouse strains, and in vitro functional assays. We propose to test the central hypothesis that macrophage function is differentially regulated by components of wood smoke via the aryl hydrocarbon receptor and NF[unreadable]B pathway.